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Hypertension and Correlation to Cerebrovascular Change: A Brief Overview
Published in Ayman El-Baz, Jasjit S. Suri, Cardiovascular Imaging and Image Analysis, 2018
Heba Kandil, Dawn Sosnin, Ali Mahmoud, Ahmed Shalaby, Ahmed Soliman, Adel Elmaghraby, Jasjit S. Suri, Guruprasad Giridharan, Ayman El-Baz
Elevated blood pressure is associated with increase in cardiovascular disease risk [4]. Table 16.3 presents the cardiovascular disease risk factors that are common in hypertensive patients. In addition, hypertension damages small and large blood vessels, including those in the brain. Conditions such as vascular dementia (sometimes called vascular neurocognitive disorder) and Alzheimer's disease have been correlated to hypertension induced changes in the cerebral blood vessels. These cerebrovascular changes develop long before symptoms appear, and thus significant vascular damage precedes diagnosis of hypertension. Functional reorganization (neuroplasticity) occurs early in the disease course, with compensatory changes including the use of more cerebral regions to complete tasks [7]. A recent study found that hypertension increases the risk for developing vascular dementia by 62% for patients between the ages of 30 and 50 and increases the vascular dementia risk by 26% for patients in the age range of 51 to 70 years old. The risk for vascular dementia is still reduced when blood pressure is lowered in older patients [8]. The risk for cognitive decline in patients with elevated systolic and diastolic blood pressures was reduced by 38% with antihypertensive therapy [9].
Physiological and pathophysiological implications of hydrogen sulfide: a persuasion to change the fate of the dangerous molecule
Published in Journal of the Chinese Advanced Materials Society, 2018
Jan Mohammad Mir, Ram Charitra Maurya
Abnormalities in the cerebral microvasculature are relevant to the cause of dementia, including AD and vascular dementia (VD). Zhang et al.[146] employed a rat model of VD by occluding bilateral common carotid artery and vertebral artery for 5 min for three times with an interval of 5 min. One month after VD induction, the number of neurons in the hippocampus was decreased and neuronal apoptosis increased. Coincidently, plasma H2S level was gradually decreased. NaHS treatment (intraperitoneal) significantly reversed neuronal injury and improved functional performance of the animals through Morris water maze. NaHS also markedly increased Bcl-2 expression and decreased Bax expression. These neuronal protective effects of exogenous H2S donor are suggestive of using H2S as a therapeutic agent for VD. They are also indicative of a neuroprotective role of endogenous H2S. In this regard, it was also found that hydroxylamine treatment (intraperitoneal) exaggerated the neuronal injury, exacerbated learning and memory, and reduced the ratio of Bcl-2/Bax in VD rats.[146] Hydroxylamine is an inhibitor of CBS. It is expected that the inhibition of CBS decreases endogenous H2S level, thus increasing neuronal apoptosis.